Sevoflurane-Induced Neurotoxicity in the Developing Hippocampus via HIPK2/AKT/mTOR Signaling View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2022-04-23

AUTHORS

Lirong Liang, Ze Fan, Danyi He, Youyi Zhao, Tian Zeng, Bing Liu, Tianyuan Ma, Junjun Kang, Hui Zhang

ABSTRACT

Sevoflurane (Sev) is a widely used inhalational anesthetic for general anesthesia in children. Previous studies have confirmed that multiple exposures to inhaled anesthetic can induce long-term neurotoxicity in newborn mice. However, the underlying mechanisms remain elusive. In this study, we investigated the role of homeodomain interacting protein kinase 2 (HIPK2), a stress activating kinase involved in neural survival and synaptic plasticity, and its underlying mechanism in sevoflurane-induced neurotoxicity. Empirical study showed that neuronal apoptosis was elevated after exposure to sevoflurane. Meanwhile, up-regulation of HIPK2 and AKT/mTOR signaling was observed in primary hippocampal neurons and hippocampus in mice upon anesthetic exposure. A64, antagonist of HIPK2, could significantly reduce increased apoptosis and activation of AKT/mTOR induced by sevoflurane. AKT antagonist MK2206 partially alleviated neuronal apoptosis without affecting the expression of HIPK2. Experimental results demonstrated a crucial role of HIPK2/AKT/mTOR signaling in neurotoxicity of sevoflurane. Thus, HIPK2/AKT/mTOR signaling can serve as a potential target for the protection of inhalation anesthesia-induced cytotoxicity in the future. More... »

PAGES

803-813

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s12640-021-00445-8

DOI

http://dx.doi.org/10.1007/s12640-021-00445-8

DIMENSIONS

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PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/35460511


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